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This Article Full Text Full Text (PDF) All Versions of this Article: 583/3/819    most recent jphysiol.2007.136309v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Saltin, B. Search for Related Content PubMed PubMed Citation Articles by Saltin, B. Related Collections Review articles

¹ Copenhagen Muscle Research Centre, University Hospital and Copenhagen University, Rigshospitalet 7652, Blegdamsvej 9, DK-2100 Copenhagen, Denmark

The primary function of the cardiovascular system is to supply oxygen to tissues and organs in the body. When muscles contract the aerobic demands are met by an increase in oxygen delivery both at the systemic and the regional levels, a match that is very close and holds at submaximal exercise and when small muscle group contract also at vigorous intensities. The level of muscle perfusion reached is 250 ml min^–1 (100 g)^–1 in muscle of sedentary subjects and in endurance-trained athletes 400 ml min^–1 (100 g)^–1 has been reported. These levels of peak exercise hyperaemia equal what has been observed in other species. One consequence of these high muscle blood flows is that the human heart cannot support an optimal blood flow in whole body exercise (arms and legs combined) and sympathetically mediated vasoconstriction, also in arterioles feeding active limb muscles, contributes to matching peripheral resistance in order to maintain blood pressure. Respiratory muscles appear to have a higher priority for a blood flow than limb and torso muscles. There is no consensus in regard to which locally produced substances elicit the vasodilatation when muscle contracts. In addition to NO, data are presented for various metabolites of arachidonic acid and also on ATP, possibly released from the red cells. Using blockers of nitric oxide synthase (L-NMMA or L-NAME) and the enzymes producing epoxyeicosatrienoic acid (EET) (sulpaphenozole or tetraetylammonium chloride) or prostaglandins (indomethacin), muscle blood flow may be reduced by up to 25–40%. Evaluating the exact role of ATP has to await further studies in humans and especially the use of specific ATP receptor blockers.

(Received 11 May 2007; accepted after revision 27 June 2007; first published online 19 July 2007)
Corresponding author B. Saltin: CMRC, Rigshospitalet 7652, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. Email: bengt.saltin{at}rh.regionh.dk

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